Abstract
The eye contains numerous water channel proteins and the roles of AQPs (aquaporins) in the retina are blurred, especially under disease conditions. The purpose of this study was to investigate the expression of AQP9 gene and proteins affected by elevated IOP (intraocular pressure) in a rat model of glaucoma induced by intravitreous injection of hypertonic saline into the episcleral veins. The gene and protein expressions of AQP9 were investigated by real-time PCR and Western blotting. The immunoreactive expression of AQP9, AQP4 and GFAP (glial fibrillary acidic protein) in the optic nerve of rats exposed to experimentally elevated IOP was detected by immunofluorescence microscopy. The mRNA and protein expression levels of AQP9 were up-regulated in the retina of an animal model of glaucoma. The immunoreactivities of the AQP9, AQP4 and GFAP were also detected and increased in the optic nerve region. The expression of AQP9 was up-regulated in this glaucoma model and the immunoreactivities of the AQP4 and GFAP were also detected as co-localizing with AQP9 in the optic nerve region, indicating retina ganglion cells were surrounded by activated astrocytes. This may indicate that the injured neurons may rely on the astrocytes. The alterations of AQP expression may compensate the glaucomatous damage.
Highlights
IntroductionGlaucoma is a group of slow progressive vision disorders affecting the trabecular meshwork, the ONH (optic nerve head) and RGCs (retinal ganglion cells) [1]
Glaucoma is a group of slow progressive vision disorders affecting the trabecular meshwork, the optic nerve head (ONH) and RGCs [1]
The mechanisms responsible for the pathophysiology of glaucoma are poorly understood, but early detection is very crucial because elevated intraocular pressure (IOP) may cause optic nerve changes that eventually lead to RGC death and glaucoma [15]
Summary
Glaucoma is a group of slow progressive vision disorders affecting the trabecular meshwork, the ONH (optic nerve head) and RGCs (retinal ganglion cells) [1]. Progressive degeneration of RGCs. Factors contributing to RGC death may include local ischaemia–hypoxia [9], excess glutamate [10], low functional cellular pumps and glutamate transporters [11], oxidative stress and free radical formation [12], inflammatory cytokines such as TNF (tumour necrosis factor) [13], abnormal immunity and secondary neurodegeneration caused by neuronal environmental changes [14]. The mechanisms responsible for the pathophysiology of glaucoma are poorly understood, but early detection is very crucial because elevated IOP may cause optic nerve changes (cupping) that eventually lead to RGC death and glaucoma [15]
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